Search results for "BRONCHOALVEOLAR LAVAGE"

showing 10 items of 105 documents

Local administration of antisense phosphorothioate oligonucleotides to the c-kit ligand, stem cell factor, suppresses airway inflammation and IL-4 pr…

2001

Abstract Background: The c-kit ligand, stem cell factor (SCF), is an important activating and chemotactic factor for both mast cells and eosinophils. These cells are known to play a fundamental role in the pathogenesis of asthma. Objective: Our goal was to analyze the functional role of SCF in the pathogenesis of asthma. Methods: The expression of SCF was targeted in fibroblasts, epithelial cells, and locally in a murine model of asthma in mice induced by ovalbumin sensitization with an antisense DNA strategy. Results: We could suppress SCF expression in NIH 3T3 fibroblasts and SP1 epithelial cells by a specific antisense phosphorothioate oligonucleotide overlapping the translation start si…

KeratinocytesLung DiseasesOvalbuminAdministration TopicalImmunologyInflammationStem cell factorBiology3T3 cellsAllergic inflammationLeukocyte CountMicemedicineImmunology and AllergyAnimalsInterleukin 4InflammationStem Cell FactorOligonucleotide3T3 CellsAllergensFibroblastsOligonucleotides AntisenseThionucleotidesMast cellAsthmaEosinophilsOvalbuminDisease Models Animalmedicine.anatomical_structureembryonic structuresImmunologybiology.proteinInterleukin-4medicine.symptomBronchoalveolar Lavage FluidThe Journal of allergy and clinical immunology
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Yttrium and lanthanides in human lung fluids, probing the exposure to atmospheric fallout.

2011

International audience; Inhalation of airborne particles can produce crystallization of phosphatic microcrysts in intraaveolar areas of lungs, sometimes degenerating into pulmonary fibrosis. Results of this study indicate that these pathologies are induced by interactions between lung fluids and inhaled atmospheric dust in people exposed to volcanic dust ejected from Mount Etna in 2001. Here, the lung solid-liquid interaction is evaluated by the distribution of yttrium and lanthanides (YLn) in fluid bronchoalveolar lavages on selected individuals according the classical geochemical approaches. We found that shale-normalised patterns of yttrium and lanthanides have a 'V shaped' feature corre…

Lanthanide010504 meteorology & atmospheric sciencesHealth Toxicology and Mutagenesis550 - Earth sciences010501 environmental sciences01 natural sciencesLanthanoid Series ElementsACTIVATED COMPLEXMass SpectrometryHuman lungLanthanideELEMENTSYttrium RadioisotopesYttriumWaste Management and DisposalLungInhalation ExposureInhalationDendriform pulmonary ossificationSEAWATERPollutionmedicine.anatomical_structureItalyEnvironmental chemistryThermodynamicsBronchoalveolar Lavage FluidAlgorithmsBronchoalveolar lavageCHEMICAL-REACTIONSEnvironmental EngineeringChromatography Gas[SDU.STU]Sciences of the Universe [physics]/Earth Scienceschemistry.chemical_elementMineralogyVolcanic EruptionsWATERSmedicinebronchoalveaolar lavagesPARTICLESEnvironmental ChemistryHumansIn patientDISSOLUTION RATES0105 earth and related environmental sciencesRARE-EARTH PNEUMOCONIOSISPrecipitation (chemistry)YttriumEnvironmental ExposureAerosolSettore GEO/08 - Geochimica E VulcanologiachemistryModels ChemicalMedical geochemistry13. Climate actionMedical geochemistry; Lanthanide; bronchoalveaolar lavagesVolcanic ashVolcanic ash
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Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

2013

Summary Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-bronchoalveolar lavages) from smokers alter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-α (PPAR-α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of i…

Leukotriene B4NeutrophilsImmunologyIntercellular Adhesion Molecule-1Blotting WesternReceptors Leukotriene B4Peroxisome proliferator-activated receptorSettore MED/41 - AnestesiologiaInflammationBronchiBiologychronic obstructive pulmonary diseasechemistry.chemical_compoundTobaccoacute lung injiurybronchial epithelial cellleukotriene B4.medicineCell AdhesionImmunology and AllergyHumansPPAR alphaReceptorPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInnate immune systemPlant Extractscigarette smokeSmokingEpithelial CellsOriginal Articlesrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1Neutrophiliarespiratory tract diseasesacute lung injiury; bronchial epithelial cells; cigarette smoke; chronic obstructive pulmonary disease; inflammation; leukotriene B4.STAT1 Transcription FactorchemistryinflammationImmunologyRespiratory epitheliumRNA Interferencemedicine.symptomBronchoalveolar Lavage FluidProtein Binding
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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

2013

Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 …

LipopolysaccharidesMaleLipopolysaccharideAcute Lung InjuryCD11cBiologyLung injuryCritical Care and Intensive Care MedicineInterleukin-23ArticleProinflammatory cytokineMicechemistry.chemical_compoundMacrophages AlveolarmedicineAnimalsInnate immune systemmedicine.diagnostic_testrespiratory systemCD11c Antigenrespiratory tract diseasesBronchoalveolar lavagechemistryImmunologyEmergency MedicineAlveolar macrophageInterleukin 17Shock
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Overview of the pathology of three widely used animal models of acute lung injury

2007

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are syndromes of acute diffuse damage to the pulmonary parenchyma by a variety of local or systemic insults. Increased alveolar capillary membrane permeability was recognized as the common end organ injury and a central feature in all forms of ALI/ARDS. Although great strides have been made in understanding the pathogenesis of ALI/ARDS and in intensive care medicine, the treatment approach to ARDS is still relying on ventilatory and cardiovascular support based on the recognition of the clinical picture. In the course of evaluating novel treatment approaches to ARDS, 3 models of ALI induced in different species, i.e. the…

LipopolysaccharidesPathologymedicine.medical_specialtyARDSSwineAcute respiratory distressLung injuryBronchoalveolar LavagePathogenesisDogsAnimalsHumansMedicineDiffuse alveolar damageIntensive care medicineLungPathologicalRespiratory Distress SyndromeSheepmedicine.diagnostic_testbusiness.industryrespiratory systemmedicine.diseaseDisease Models AnimalBronchoalveolar lavageSurgerybusinessOleic AcidAcute diffuse
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Evaluation of soluble CD 14 and neopterin as serum parameters of the inflammatory activity of pulmonary sarcoidosis.

1992

CD14 represents the most specific marker for monocytes/macrophages. It has been demonstrated in vitro that monocytes/macrophages lose this antigen upon activation. Results of studies investigating the expression of membrane-bound CD14 on the surface of monocytes/macrophages in sarcoidosis patients are controversial. To investigate whether the soluble form of CD14 reflects monocyte/macrophage activation in sarcoidosis, serum levels of soluble CD14 were determined concurrently with other serum markers of monocyte/macrophage activation (neopterin, angiotensin-converting enzyme) in 50 consecutive patients with bioptically confirmed sarcoidosis. The patients were allocated to three groups accord…

Lung Diseasesmedicine.medical_specialtySarcoidosisCD14CD4-CD8 RatioLipopolysaccharide ReceptorsAntigens Differentiation MyelomonocyticPeptidyl-Dipeptidase ANeopterinSensitivity and SpecificityMonocyteschemistry.chemical_compoundImmune systemAntigenAntigens CDInternal medicineDrug DiscoverymedicineMacrophageHumansGenetics (clinical)Inflammationmedicine.diagnostic_testMonocyteNeopterinGeneral MedicineMacrophage Activationmedicine.diseaseBiopterinBronchoalveolar lavageEndocrinologymedicine.anatomical_structurechemistrySolubilityImmunologyMolecular MedicineInterleukin-2SarcoidosisBronchoalveolar Lavage FluidBiomarkersThe Clinical investigator
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Alveolar macrophage dynamics in murine lung regeneration

2012

In most mammalian species, the removal of one lung results in dramatic compensatory growth of the remaining lung. To investigate the contribution of alveolar macrophages (AMs) to murine post-pneumonectomy lung growth, we studied bronchoalveolar lavage (BAL)-derived AM on 3, 7, 14 and 21 days after left pneumonectomy. BAL demonstrated a 3.0-fold increase in AM (CD45(+), CD11b(-), CD11c(+), F4/80(+), Gr-1(-)) by 14 days after pneumonectomy. Cell cycle flow cytometry of the BAL-derived cells demonstrated an increase in S + G2 phase cells on days 3 (11.3 ± 2.7%) and 7 (12.1 ± 1.8%) after pneumonectomy. Correspondingly, AM demonstrated increased expression of VEGFR1 and MHC class II between days…

MHC class IIeducation.field_of_studyLungbiologymedicine.diagnostic_testPhysiologymedicine.medical_treatmentClinical BiochemistryPopulationCD11cCell Biologyrespiratory systemFlow cytometryAndrologyPneumonectomyBronchoalveolar lavagemedicine.anatomical_structureImmunologyAlveolar macrophagebiology.proteinmedicineeducationJournal of Cellular Physiology
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Pulmonary cytomegalovirus (CMV) DNA shedding in allogeneic hematopoietic stem cell transplant recipients: Implications for the diagnosis of CMV pneum…

2019

Highlights • CMV DNA is frequently detected in BAL fluid specimens from allo-HSCT. • CMV DNA detection in BAL fluids is comparable across pneumonia etiologies. • CMV DNA loads in BAL fluids are comparable across pneumonia etiologies. • CMV DNA load in BAL may predict attributable-pneumonia mortality.

Male0301 basic medicineDna loadCMV pneumoniaCytomegalovirusmedicine.disease_causechemistry.chemical_compound0302 clinical medicinePre-emptive antiviral therapyMedicine030212 general & internal medicineCMV DNA in BALAged 80 and overmedicine.diagnostic_testHematopoietic Stem Cell Transplantationvirus diseasesrespiratory systemMiddle AgedViral LoadVirus SheddingInfectious DiseasesCytomegalovirus InfectionsFemaleAllogeneic hematopoietic stem cell transplantBronchoalveolar Lavage FluidAdultMicrobiology (medical)Pneumonia Viral030106 microbiologyCMV DNAemiaArticle03 medical and health sciencesHumansTransplantation HomologousAgedRetrospective Studiesbusiness.industryCMV PneumoniaCytomegalovirusRetrospective cohort studymedicine.diseaseTransplant Recipientsrespiratory tract diseasesPneumoniaBronchoalveolar lavagechemistryDNA ViralImmunologybusinessDNAJournal of Infection
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Community-acquired respiratory virus lower respiratory tract disease in allogeneic stem cell transplantation recipient: Risk factors and mortality fr…

2018

Abstract Risk factors (RFs) and mortality data of community‐acquired respiratory virus (CARVs) lower respiratory tract disease (LRTD) with concurrent pulmonary co‐infections in the setting of allogeneic hematopoietic stem cell transplantation (allo‐HSCT) is scarce. From January 2011 to December 2017, we retrospectively compared the outcome of allo‐HSCT recipients diagnosed of CARVs LRTD mono‐infection (n = 52, group 1), to those with viral, bacterial, or fungal pulmonary CARVs LRTD co‐infections (n = 15, group 2; n = 20, group 3, and n = 11, group 4, respectively), and with those having bacterial pneumonia mono‐infection (n = 19, group 5). Overall survival (OS) at day 60 after bronchoalveol…

Male0301 basic medicinemedicine.medical_treatmentcommunity acquired respiratory virusHematopoietic stem cell transplantationBronchoalveolar LavageGastroenterology0302 clinical medicineRisk Factorsrespiratory virus co‐infectionsLungRespiratory Tract Infectionsmedicine.diagnostic_testRespiratory tract infectionsCoinfectionHematopoietic Stem Cell TransplantationMiddle AgedCommunity-Acquired InfectionsInfectious Diseasesmedicine.anatomical_structureVirusesvirus-bacterial mixed infectionsRespiratory virusFemaleOriginal Articlerespiratory virus co-infectionsBronchoalveolar Lavage FluidAdultmedicine.medical_specialtyvirus‐bacterial mixed infections030106 microbiologyContext (language use)CMV DNAemiaAntiviral Agents03 medical and health sciencesInternal medicinemedicineHumansTransplantation Homologousallogeneic hematopoietic stem cell transplantationAgedRetrospective StudiesTransplantationLungBacteriabusiness.industryFungiBacterial pneumoniaOriginal Articlesmedicine.diseaseTransplantationBronchoalveolar lavagebusinessimmunodeficiency score index030215 immunology
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Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model.

2018

INTRODUCTION:The acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a "lung-brain-crosstalk". Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage. METHODS:After approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of …

MaleARDSCritical Care and Emergency MedicinePulmonologySwinePhysiologymedicine.medical_treatmentVentilator-Induced Lung InjuryInterleukin-1betalcsh:MedicineApoptosisPathology and Laboratory MedicineHippocampusPositive-Pressure RespirationRandom Allocation0302 clinical medicineAnimal CellsImmune PhysiologyMedicine and Health Scienceslcsh:ScienceImmune ResponseAcute Respiratory Distress SyndromeTidal volumeCerebral CortexNeuronsCognitive ImpairmentRespiratory Distress SyndromeInnate Immune SystemMultidisciplinarymedicine.diagnostic_testCognitive NeurologyBrainGeneral MedicineLung InjuryNeurologyAnesthesiaBreathingCytokinesTumor necrosis factor alphamedicine.symptomAnatomyCellular TypesGeneral Agricultural and Biological SciencesResearch ArticleHistologyCognitive NeuroscienceImmunology10208 Institute of NeuropathologyInflammation610 Medicine & healthGenetics and Molecular BiologyGlial Cells1100 General Agricultural and Biological SciencesLung injury03 medical and health sciencesSigns and SymptomsRespiratory Failure1300 General Biochemistry Genetics and Molecular BiologyDiagnostic MedicinemedicineAnimalsMicroglial CellsMechanical ventilationInflammation1000 Multidisciplinarybusiness.industryInterleukin-6Tumor Necrosis Factor-alphalcsh:RBiology and Life Sciences030208 emergency & critical care medicineCell BiologyMolecular Developmentmedicine.diseaseRespiration ArtificialBronchoalveolar lavage030228 respiratory systemImmune SystemCellular NeuroscienceGeneral Biochemistry570 Life sciences; biologyCognitive Sciencelcsh:QbusinessDevelopmental BiologyNeurosciencePloS one
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